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	<title>Comments on: Obesity prevalence: nothing new but something weird</title>
	<link>http://pharmaweblog.com/blog/2006/09/15/obesity-prevalence-something-weird/</link>
	<description>Pharmaceutical and biotech science and business</description>
	<pubDate>Thu, 28 Aug 2008 20:08:20 +0000</pubDate>
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		<title>by: Pharma&#8217;s Cutting Edge &#187; New evidence linking viruses to obesity</title>
		<link>http://pharmaweblog.com/blog/2006/09/15/obesity-prevalence-something-weird/#comment-81</link>
		<pubDate>Tue, 21 Aug 2007 16:49:22 +0000</pubDate>
		<guid>http://pharmaweblog.com/blog/2006/09/15/obesity-prevalence-something-weird/#comment-81</guid>
					<description>[...] Last September, I noted that the epidemiology of modern obesity (in the last couple decades) strongly suggests transmissible or pervasive environmental factors&amp;#8211;more persavive even than junk food and sedentary behavior&amp;#8211;at work in its etiology.  Now, Magdalena Pasarica, M.D., Ph.D., of the Pennington Biomedical Research Center and her colleagues are reporting at the American Chemical Society meeting that adenovirus-36 (Ad-36), a common form of this common human-infecting virus, is capable of differentiating adult human stem cells into fat: In the current study, Pasarica and her associates obtained adult stem cells from fatty tissue from a broad cross-section of patients who had undergone liposuction. Half of the stem cells were exposed to Ad-36 and the other half were not exposed to the virus.  After about a week of growth in tissue culture, most of the virus-infected adult stem cells developed into fat cells, whereas the non-infected stem cells did not, the researchers say.  Funded by the National Institutes of Health (NIH), Dr. Dhurandhar’s group recently identified a gene in the Ad-36 virus that appears to be involved in causing fat accumulation observed in infected animals. That gene, called E4Orfl, is now emerging as a promising target for future human therapies, such as vaccines and anti-viral medicines, aimed at preventing or inhibiting the obesity virus, she says. [...]</description>
		<content:encoded><![CDATA[<p>[&#8230;] Last September, I noted that the epidemiology of modern obesity (in the last couple decades) strongly suggests transmissible or pervasive environmental factors&#8211;more persavive even than junk food and sedentary behavior&#8211;at work in its etiology.  Now, Magdalena Pasarica, M.D., Ph.D., of the Pennington Biomedical Research Center and her colleagues are reporting at the American Chemical Society meeting that adenovirus-36 (Ad-36), a common form of this common human-infecting virus, is capable of differentiating adult human stem cells into fat: In the current study, Pasarica and her associates obtained adult stem cells from fatty tissue from a broad cross-section of patients who had undergone liposuction. Half of the stem cells were exposed to Ad-36 and the other half were not exposed to the virus.  After about a week of growth in tissue culture, most of the virus-infected adult stem cells developed into fat cells, whereas the non-infected stem cells did not, the researchers say.  Funded by the National Institutes of Health (NIH), Dr. Dhurandhar’s group recently identified a gene in the Ad-36 virus that appears to be involved in causing fat accumulation observed in infected animals. That gene, called E4Orfl, is now emerging as a promising target for future human therapies, such as vaccines and anti-viral medicines, aimed at preventing or inhibiting the obesity virus, she says. [&#8230;]
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